Good morning, and welcome, ladies and gentlemen, to Cytokinetics Conference Call. At this time, I would like to inform you that this call is being recorded and that all participants are in a listen only mode. At the company's request, we will open the call for questions and answers after the presentation. I will now turn the call over to Diane Weiser, Cytokinetics' Vice President of Corporate Communications and Investor Relations. Please go ahead.
Good morning, and thank you for joining us on the call today. Robert Blum, our President and Chief Executive Officer, will lead with an overview of Saturday's announcement. Then Fady Malik, our EVP of Research and Development, will provide a brief background on reldesemtiv and our Phase I data before Doctor. John Day recaps key findings from the recently presented Phase 2 study of reldesemtiv in patients with SMA. Robert will provide some closing remarks before we open the call to questions.
Andy Wolf, our Chief Medical Officer and Qing Jia, our Chief Financial Officer are also with us on the call to participate in the Q and A. Portions of the following discussion, including our responses to questions, contain statements that relate to future events and performance rather than historical facts and constitute forward looking statements for purposes of the Safe Harbor provisions of the Private Securities Litigation Reform Act of 1995. Examples of forward looking statements may include statements relating to the potential benefits of reldesemtiv and patients with SMA, our strategic initiatives, our collaboration with Astellas, clinical trials and the potential for eventual regulatory approval of our product candidates, including reldesemtiv. Our actual results might differ materially from those projected in these forward looking statements. Additional information concerning factors that could cause our actual results to differ materially from those in these forward looking statements is contained in our SEC filings, including our most recent 10 ks, 10 Q and 8 ks.
We undertake no obligation to update any forward looking statements after this call. And now, I will turn the call over to Robert.
Thank you, Diane, and thanks again to everyone for joining us on the call today. This past Saturday, June 16, Cytokinetics announced that data from the Phase 2 clinical study of reldesemtiv in patients with spinal muscular atrophy or SMA were presented by Doctor. John Day, Professor of Neurology and Pediatrics at Stanford at the 2018 Annual Curesma Conference in Dallas. We're very pleased to have Doctor. Day on the call with us this morning.
Thank you, John for joining us. As our press release stated, we believe that this hypothesis generating study met its primary objective to determine potential pharmacodynamic effects of reldesemtiv after multiple oral doses in patients with SMA, as well as secondary objectives to evaluate the safety, tolerability and pharmacokinetics of reldesemtiv. As you know, we're developing reldesemtiv in collaboration with Astellas as a potential treatment for people with SMA, as well as certain other disability diseases and conditions associated with skeletal muscle weakness and or fatigue. As John will elaborate, the study showed dose and concentration dependent increases in time to muscle fatigue as measured by changes from baseline in 6 minute walk distance, a submaximal exercise test of aerobic capacity and endurance and maximal expiratory pressure or MEP, a measure of strength of respiratory muscles in both cases after 8 weeks of treatment with reldesemtiv. As some of you know, the Cure SMA meeting is a special meeting providing a rare opportunity for researchers and industry to meet directly with patients and loved ones courageously living with SMA and to share updates on clinical progress.
We were pleased to share the results of this study with the SMA community as we believe this study provides the first data indicating that a muscle directed therapy, namely a fast skeletal muscle troponin activator or FASTA may hold promise for potential clinical benefit for patients with SMA. With that, I'll turn it over to Fady to remind you of the mechanism of reldesemtiv and recap some key findings from the Phase 1 clinical trials program that inform the design of our study in SMA.
Thanks, Robert. The reldesemtiv is a next generation fast skeletal muscle troponin activator or FASTA. As you'll recall, it has the same mechanism as tirzemtiv, but was selected and optimized from a different and distinct chemical series. As we found in our Phase 1 clinical trials program, reldesemtiv may have a more favorable tolerability profile relative to tirasemtiv with regard to lightheadedness and other potential adverse effects. The most telling Phase 1 study looked at the pharmacodynamic effects in healthy volunteers and was similar to a previous study conducted with Tirasemtiv.
In this study, we stimulated the deep fibular nerve which runs on the outside of the knee and controls the tibialis anterior muscle in the front of the leg. The force produced during stimulation of the nerve was measured before and at several times points after doses single doses of reldesemtiv were administered to healthy subjects. We found the magnitude of response was twice as large over a range of plasma concentrations that was approximately half that which we observed with tirasemtiv. This is largely because reldesemtiv is less protein bound and therefore penetrates muscle more effectively producing a larger effect. Additionally, the tolerability issues observed with tirasemtiv in Phase 1 were not observed with reldesemtiv.
Based on the results presented this weekend, it seems the tolerability and side effect profile of reldesemtiv as well as its impact on muscle force, power and stamina may be translating to patients with SMA as evidenced by the improvements observed in 6 minute walk But before that, I'll review a couple of key slides with regards to the mechanism of actions and the Phase 1 data. Turning to the slide deck on Slide 2, just to remind you, reldesemtiv is a selective small molecule activator of the troponin complex in skeletal muscle. It increases the affinity of the troponin complex for calcium and thus sensitizes the sarcomere to calcium and nerve input, which causes the release of calcium inside of muscle to activate muscle. The next slide shows some preclinical work that was done in 2 models of spinal muscular atrophy. The one on the left is a more severe model.
You can see that stimulating nerve to the leg muscles there results in a certain amount of force in the control animals on the left and the gray bar. And in the blue bar, these animals are much weaker, with only about 20% of the force of their controls being produced by the same nerve stimulation. Administration of reldesemtiv at 2 doses increases the amount of force produced in the green bars. And on the right, it shows a less severe model of SMA, again with somewhat reduced force at baseline. And here reldesemtiv producing greater forces at the same nerve stimulation rates as were done in the control and vehicle treated animals.
The next slide shows translation of this mechanism of action into humans in a similar experiment in which reldesemtiv was administered to healthy volunteers in 3 doses and also placebo was given. The doses were administered in a random fashion and also blinded, of course, to both the investigator and the subjects. The fibular nerve there was stimulated, eliciting an increase in force, dorsoflexion of the foot. And again, what you see here are concentration dependent increases in force, subsequent to the dosing of reldesemtiv. The doses that we studied in CY-five thousand and twenty one we're expected to produce plasma concentrations in the lower and higher range of pharmacodynamic effect observed in this slide, which is important as we go on as Doctor.
Day will point out. So with this translation of mechanism into humans, we embarked on conducting study CY-five thousand and twenty one in patients with SMA. And now I'll turn it over to Doctor. Day, who will present the study results. Great.
Thanks, Fady. So we're
up to Slide 5. And basically this is a hypothesis generating study that we devised to investigate the effects of reldesemtiv in SMA. Slide 6 sketches out a little bit more about this study that was really designed to study the pharmacokinetic and pharmacodynamic and safety features in 2 cohorts dosed at 1 Importantly, in the inclusion and exclusion criteria, Importantly, in the inclusion and exclusion criteria, we were studying an older age group than is studied in most SMA studies, looking at types 2, 3 and 4 and use the Hammersmith functional motor score to identify the appropriate population, excluding patients that were either too weak and had a Hammersmith less than 10 or too strong and had a Hammersmith greater than 54. That will come back in terms of the population that we studied as evidenced on the next slide. Next slide.
So this just shows the construct of the study again where we had 2 cohorts, the low dose and the high dose, trying to maintain equal numbers of ambulatory and non ambulatory patients and then randomizing at a 2:one treated to placebo ratio for those groups. The subsequent Slide 8 shows the intensity of this study. So it was at most 15 weeks. But during that time, they had patients had 7 study visits so that we followed them quite closely. It should be pointed out that the final data lock will actually be later this week as we collect the last data on the follow-up visits.
And on Slide 9, you can see the outcome measures that we used. Again, pointing out the various measures that we followed during this. The one point here is that the SMA Health Index was only available to us for cohort 2. That was not yet available for us the low dose cohort. And then in terms of the actual patients that we enrolled, you can see that we enrolled on the left 39 subjects in cohort 1 and on the right 31 in cohort 2.
We maintained a fairly good balance between ambulatory in green and non ambulatory in blue. As evidenced on the slide in cohort 1, we had 2 early terminations, but both were from the placebo arm of that cohort due to adverse events that occurred in those subjects. In Cohort 2, we had 3 early terminations, 1 due to a protocol deviation and 1 because they withdrew for another study, 1 due to an adverse event as we'll discuss. In terms of the demographics, there were no significant differences between the 3 groups of placebo, low dose and high dose cohorts. You will note that most of the patients ended up being of Type 3, even though type 2, 3 and 4 were opened for enrollment.
Type 2 patients by and large were too weak and had Hammersmiths below 10 and Type 4 patients were all too strong having Hammersmith's greater than 54. In the next slide, you can see the baseline characteristics. And again, there was no significant difference between the groups in these measures going into the trial. Again, pointing out that the SMA high or SMA health index was not available to us for that low dose cohort. Slide 13, I think we're up to, shows a forest plot of a lot of the results.
And you can see that many of the study parameters did not change. On the left, you can see the low dose cohort and on the right, the high dose cohort points that tend to favor placebo, edge to the left of the median line and towards reldesemtiv to the right. But 2 particular parameters stand out, namely the maximum expiratory pressure, MEP and the 6 minute walk distance. And you can see in this overall graph of all participants, there does seem to be a dose dependent increase in effect in those two parameters for both maximum expiratory pressure and 6 minute walk distance. We pulled out the 6 minute walk distance to look at a little bit more closely and this shows the effect over time for that measure in the gray line showing the placebo group, the light green, the low dose cohort and the dark green, the high dose cohort showing again evidence of a fairly clear dose response improvement in the 6 minute walk distance.
And the waterfall plot reiterates that point again showing several individuals having a significant improvement on the high dose tendency for the placebo patients to have little effect or deteriorate and the lower dose cohort to be in the middle. And then graphing this out versus the drug exposure on the x axis there in Slide 16, you can see the peak plasma concentration measured during pharmacokinetic studies on the same day as these 6 minute walk distances were measured, showing a fairly significant dose relationship between the increase in 6 minute walk distance with a p value for this of less than 0.01. I'll point out, I should go back to that slide, if you take me back, Diane. So on Slide 16, you can see that even the highest concentration, there was less than 5. And if we look at the quartiles, the highest dose quartile was significantly less than the target of 7 6 or 7 micrograms per milliliter.
On the next slide, you can see again what Fady had pointed out in terms of the study of control subjects earlier. Our target range for the high dose was in the upper end of that dose response curve and we did not achieve that, which we assume is due to a change in drug formulation. You can see the graded box there showing the hoped for range of exposure and the green box at 3 to 4 micrograms per milliliter shows the concentration actually achieved in the top quartile of the patients in 5,021. In terms of side effects, there were no significant AEs that differentiated between the placebo low dose and high dose subjects. The most common adverse events were headache and gastrointestinal issues, but those were fairly similar between the different cohorts and no other significant toxicity was identified.
In terms of serious AEs, there were 4 subjects that experienced serious AEs, none of which were thought to be related to drug. 3 of them had clearly superimposed problems, the salmonella, facial pain and a fall and fracture. The 4th subject had elevated serum creatine phosphokinase that was attributed to his at the end of the treatment period becoming overly active and undertaking a significant home improvement episode and apparently had a transient CK elevation at that time. It did not affect his treatment with the drug and resolved spontaneously. So in conclusion, we think that this hypothesis generating study is seeming to show some indication of muscle directed improvement relevant to the SMA population, namely in terms of 6 minute walk distance and maximum expiratory pressure.
We note that there was no efficacy plateau demonstrated. So we think that there is likelihood that increasing the drug exposure can further amplify this response. And we believe that the lower than expected drug exposure is attributed to a change in drug formulation that can be rectified with increased dosing. There were no safety or tolerability issues that would prevent us from doing that. So in essence, I think that the study did its job in generating some valid hypotheses that can be explored further with this compound.
So thank you very much for the opportunity to go over this with you.
Thank you, John. So these are very exciting times and optimistic times for the SMA community. The future for patients living with SMA today is brighter than ever with the recent introduction of gene directed therapies. Today, it's expected that patients may live longer with the advent of new therapies, but still have a significant unmet need sorry, today is expected that patients may live longer with the advent of new therapies, but will still have a significant unmet need with expected disabilities related to respiration and mobility. So we estimate 50% of type 3 patients with SMA are believed to maintain ambulatory function today and an increasing number of type 2 patients with SMA are expected to remain ambulatory with the advent of complementary new therapies that can enable motor milestones.
Over the next 5 years, the prevalence of ambulatory adolescents and adults with SMA may exceed 5000 to 10000 patients in the United States alone. While we did not see effects on all of the assessments explored in this Phase 2 hypothesis generating study, that was to be expected and we're encouraged to see that treatment with reldesemtiv produced dose and concentration dependent clinically meaningful benefits in 6 minute walk distance as well as maximal expiratory pressure. With these data in hand together with our partner Astellas, we'll be evaluating potential next steps in the development plan for reldesemtiv. Once we've completed a full analysis of the clinical study data, we'll seek guidance from the SMA community, clinical experts in SMA and regulatory authorities as may inform a potential path forward for this drug candidate. We look forward to continuing our analyses and charting a path forward for reldesemtiv as we await results from the additional trials in COPD, ALS and elderly subjects with limited mobility, all part of our broad mid stage development program in collaboration with Astellas.
We remain optimistic about the promise and potential of this drug candidate and we look forward to keeping our partners in the disease communities and our shareholders apprised of our progress. Operator, with that, we can now open up the call to questions, please.
Your first question comes from the line of Matthew Harrison with Morgan Stanley.
Good morning, Matthew.
Great. Good morning. Thanks for taking the questions. I think 2 for me, if possible. So the first one, maybe for Doctor.
Day, maybe you could just comment a little bit on where you might if this therapy can demonstrate a benefit in 6 Minute Walk, where would you think this will fit in the treatment paradigm given what we've seen from some of the other agents on the market? And then a second one for the company, maybe you could just also remind us, given the dose exposure levels that you've seen, what that means for some of the other studies that you're running with reldesemtiv? Thanks.
Excellent. John, maybe I'll defer to you for the first question and Fady to you for the second.
Sure. So as you may be aware for in SMA, we've long been seeking somewhat symptomatic treatments as well as these disease modifying treatments that you allude to that are now being increasingly made available. So, I think that this can function as a very significant add on to those treatments. The hope is that patients will improve with the SMN protein modifying treatments, but very, very few of those patients are actually normal. Almost all of them have residual motor deficits.
And I think that coming up with a mechanism to improve their efficiency of force generation will definitely be something that will have a place in the entire SMA community.
I'll take the same part of the question. As we mentioned, we think we have room to move higher in this study, but the range of exposures that we achieved are still quite substantially pharmacodynamically active and more so when compared to tirasemtiv, which we studied in ALS. And so we think the ALS study is doses that we selected and exposures that we'll observe are sufficient for us to confirm the hypothesis that we laid out in that study, which is that reldesemtiv will slow the decline and slow vital capacity as we observe with tirasemtiv.
Great. Thanks very much.
Thank you, Matthew.
Your next question is from the line of Chad Messer with Needham.
Good morning, Chad.
Good morning. Thanks for taking my question and congrats on the encouraging data, particularly with regards to safety, tolerability and 6 minute walk. Given that this was a hypothesis generating study, I wonder if you guys have any mechanistic hypotheses as to why we're seeing this effect on maximal expiratory pressure in the non ambulatory patients and then not in the ambulatory ones and then perhaps some difference to the two diseases. Just wanted to get your thoughts on that.
I'll start and then I'll ask Fady to speak about what we know regarding maximal expiratory pressure or MEP and what that's measuring and why that may translate to the properties of reldesemtiv and maybe ask Andy also to step in and remind everyone on the call about some of the data we had generated early on with tirasemtiv in terms of this mechanism and extending time to muscle fatigue across a broad array of other populations with muscle weakness. So Fady, do you want to start?
Yes. So I think, we observed improvements in MEP in both populations. The effects were greater in the non ambulatory population and the baseline data in those groups was substantially lower. They had lower MEPs at baseline and thus had more headroom to improve. The maximum expiratory pressure is a maneuver that takes and it requires the diaphragm, the abdominal muscles, the chest wall muscles.
It's a somewhat sustained effort over a few seconds that is potentially correlated with patient's ability to cough and other things. So we think of it as a measure of muscle function that is confirmatory. The effects on forced vital capacity, we didn't see, but the baseline forced vital capacity in these patients is close to normal, about 85% of predicted, although you have to recognize that predicted is based on healthy volunteers with normal body habitus and normal thoracids and so forth, which these patients often don't have, given their scoliosis and other skeletal muscle or skeletal deformities. So I think it's a confirmatory signal. The 6 minute walk distance is a much different kind of metric that looks more fatigability with repetitive movements over 6 minutes.
And maybe I'll turn it over to Andy who can talk about a little more development experience with tirasemtiv in that regard. Well, potentially,
I think what Robert was referring to is why 6 minute walk among some of the other tests. And one thing that can improve 6 minute walk distance is diminished fatigue ability. It's obviously something that occurs over an extended period of time. And with tirasemtiv, our first fast skeletal muscle troponin activator, you may recall that we did a study in myasthenia gravis where we saw significant improvements in the QMG score. But when you look at those data, some of the most prominently affected components of that score were those that were related to endurance and not maximal effort, how long a person could hold their head up off of a supine position, for example, or hold their arm out from their body.
We also did a similar earlier study with tirasemtiv in patients with claudication, in their calf muscle where we asked them to do heel lifts where they went up on their toes as high as they could and came back down. And they did that every other second. There was a metronome. And we could measure the angle of the elevation and we weighed them as well. So we could calculate the actual work that, that claudicating muscle did before it finally fatigued.
And we saw that with tirasemtiv patients did significantly more work. So they went higher for a longer period of time before they finally did have to stop because of either intolerable pain or just inability to do it. So there's a prominent anti fatigability effect of the drug, and we knew that from preclinical data as well.
Okay, great. That's all actually very helpful and makes sense. Maybe just one more on formulation. It sounds like you guys were kind of surprised or mispredicted what kind of exposure you would get with this formulation. Where are you in terms of finalizing formulations and what work you need to do here?
Or are you fairly confident that you'll have enough data to basically design for your studies.
Sure. I'll mention a couple of things already and then maybe Fady can elaborate if necessary. The formulation development work is a continuing process that has already been underway with our colleagues at Astellas that there are new process development and new formulation sciences activities that got started well before we had these data in anticipation of taking forms into pivotal studies that would address not only some of the issues that you've heard about, but also help to ensure that we have better cost of goods and other efficiencies and optimized processes for what could ultimately be commercial scale manufacturing. So it's a continuum and we're already deep into those activities.
Yes. I'll just maybe expand in that. The increase between 150 milligrams and 450 milligrams twice a day in the study was linear. We got about 3 fold the exposure for 3 fold the dose. And seen that at higher doses as well in healthy volunteers.
And so one approach is simply to increase the dose and we would expect exposure increase. At the same time, we will conduct in parallel formulation development activities to try and optimize the exposure of reldesemtiv.
Okay, thanks. Look forward to hearing a lot more about reldesemtiv in the future.
Thank you, Chad.
Your next question is from the line of Joe Pantginis with H. C. Wainwright.
Good morning. Hey, guys. Good morning. Thanks for taking the question. First question, maybe for Doctor.
Day, with the premise that these data have very limited comparators with SPINRAZA or nusinersen being the only drug on the market, Can you talk to the appropriateness even of using the Hammersmith scale in this population because nothing was seen in this study for Hammersmith, whereas it's in the label based on study 2 for SPINRAZA. So again, can you just discuss even the appropriateness of using Hammersmith for this population? Thanks.
Yes, John, I'll turn that to you.
Okay. So I think several points. I mean, the Hammersmith was really devised for infants and young children. And consequently, using it for this population is questionable to start with. We used it because of the familiarity of the therapist with it and because we did think it would stratify the population well.
But as in terms of an outcome measure going forward, I think it probably will prove itself to be not something that measures more stamina than just simply power production, which in essence that is what the Hammersmith is doing.
No, that's very helpful. Thank you. And then, with regard to the 6 minute walk distance, I just had a quick question with regard to the placebo responses. Is this considered, I guess, any regard to say a training effect in these patients or do you consider it just noise?
In the placebo? I mean, there's a lot of randomness, I mean, inevitably in doing the 6 minute walk test. And so I think that that's always a factor when we do this. There's but I think there in this instance, we did see an increase of at different points, tens of meters in different subgroup analyses upwards of 60 meters in some groups. And that's beyond the noise level when we're looking at it that way.
So I think it's very hard to look at the 6 minute walk distance in individuals, but in group data like this, that degree of differences is greater than expected. So that we usually use a cutoff of 30 meters as being more than we would expect to see in group data and we were getting beyond that in some of the group analyses.
Great. Thank you very much.
Thank you, Joe.
Your next question is from the line of Mara Goldstein with Cantor Fitzgerald.
Thank you.
Good morning, Mara.
Good morning. So, just a question. So the 6 minute walk test and, MEP were positive parameters, while mostly others were largely unchanged with the exception of the muscle mega score, which had a very distinctly different, if you will. I know certainly don't want to say pattern because I understand it's a small trial, but it did favor placebo in the ambulatory high dose. And maybe can you just provide some rationale for why these figures are appearing for this particular parameter test parameter?
So that's a very good question. And I think, while I'll adjust maybe we're seeing a trend, I wouldn't suggest that there was a meaningful finding there. Certainly, it's left leaning towards favoring placebo, but not otherwise deemed statistically significant. But Fady and Andy may have explanations they can share.
Thank you.
I think there are 2 things to consider. 1 is when we looked at the individual data there, there were a couple of placebo patients whose strengths improved rather remarkably over the course of the study. And that is as measured, I say, because this measurement is dependent both on the patient and the evaluator conducting this. And sometimes the evaluators in this area where muscle mega score is not used, the spinal muscular atrophy was not used regularly, I think potentially we had some evaluators across sites that were not as experienced as other evaluators. It's used more frequently in ALS and centers are I think more used to using it there and we try to employ it here in SMA to see how it would work.
But John can comment on how often placebo patient strength improves by that degree that we observe in
some of
the individuals. Yes, I
mean, it's again quite variable and depends a lot on the technique of the investigator as well as various motivational issues that can creep in if somebody isn't feeling well or is exhausted or whatever. So I think that we don't we have to look at those individuals a little bit more closely and see if their initial values were low or if their subsequent values were high or whatever. I don't put a lot of stock in it because of that. And again, for the most part, this is more of a measure of muscle force than of stamina. And I think that we need to look and see whether or not that is something that we want to even consider going forward.
Okay. And if I can also just ask Doctor. Dave from a practical perspective, when you think about the idea around either combination or treatment with reldesemtiv and other agents like SPINRAZA. At this point, I understand it's early on, but how would you potentially think that reldesemtiv would be incorporated into a sort of SPINRAZA treated world?
Yes, I think that's a great question. I think it's illustrative perhaps to look at the AveXis experience where a significant number, I keep hearing various numbers of patients treated with AveXis have then subsequently been treated with SPINRAZA. And I think what that's saying is that there is a residual deficit there that the motor improvement is not absolute. And consequently, these patients have residual need. My guess is that, you're going to max out in terms of the effects of SMN protein up regulation and it's not a matter of just continuing to increase that, that you need something beyond SMN protein up regulation.
So I think there's already a significant need in terms of developing muscle directed therapies that are going to augment the effects of these SMN protein regulators. So I think it will have a place. I think it will be very clear in patients that there is value of this type of treatment on top of the SMN protein up regulation approach.
Okay. Thank you.
Your final question is from the line of Vernon Bernardino with Seaport Global.
Good morning, Vernon.
Good morning and congrats again on the results. Thanks for taking my question. Two questions. If you look back on Slide 16 and the result on 6 Minute Walking Distance, So there's great variability. Obviously, it's not a very large study in the results.
Perhaps, Doctor. Day, as far as you've seen, over time, at least with the placebo results, do you expect that the performance of these patients perhaps get tighter over time beyond week 8? And I guess for Robert and the team, do you expect with a larger study and then higher doses that you would see a tighter result and continued improvement in our walking distance?
John, we'll start with you.
So again, looking at individual data in report data on individual subjects just for that reason. We always look at group data for this. So, I do expect that there will always be some degree of noise, but I do think that the divergence would become more clear with larger end here that there's going to be a significant difference that that will be evident. I think already the P values are fairly significant for even the small group. So I'm fairly optimistic that we'll see it more clearly in the larger group.
And maybe just to elaborate, if I may. We've consistently seen with this mechanism of fast skeletal troponin activators, dose dependent and exposure driven increases in muscle force, muscle power and time to muscle fatigue. And therefore, we don't expect that there's a difference in this study between what was observed at week 4 and what was observed week 8 in terms of magnitude of effect for any of the dose levels. What will be interesting to see is in future studies as we may be able to now achieve higher exposures, whether we see and I expect we may significantly increased effects with increasing exposures and whether that may translate to cumulative effects over time or just maintained effect consistent with exposure. I think that'll be a key question that we'll want to investigate with potentially further studies.
You had another question?
Yes. Thank you. Second question, Doctor. Dave, in any of the other outcome measures, were there ones would you like to have seen positive results or at least significantly positive trends?
I mean, this really was for me a hypothesis generating study, so that I didn't start out with any significant preconceived notions about where we were going to see the effects. I think it makes sense that we're seeing it in a 6 minute walk distance. I think that the expiratory pressure also makes some sense. That's a very complex move that's utilizing a group of muscles, some of which are more and less affected in SMA. So I think intriguing and one that we're going to want to dive into a little more.
The other outcome measure I'm interested in is the patient reported outcome measure that if the SMA high really did allow us to capture this. At present, we're looking for measures of stamina. Those might be the best ones that would indicate an effect.
There are no further questions.
Thank you, operator. And thank you to all of the participants on our teleconference today. Thank you for your continued support and interest in cytokinetics. These data with reldesemtiv in patients with SMA represent for us a dawn of a new day in light of some of the disappointments admittedly regarding tirasemtiv and its tolerability profile. Certainly, these data suggest that reldesemtiv consistent with the therapeutic hypothesis may be more well tolerated than tirasemtiv not only in this population, but in others.
And certainly with these data underscoring increases in time to muscle fatigue as measured by 6 minute walk distance, a measure that we think has applicability to not only this population, but potentially others. These are encouraging data around which we hope to be able to now provide further support for this program moving forward. That together with our partners at Astellas and after further discussions with the SMA community and with regulatory authorities. So we thank everybody for their interest and attention this morning. With that operator, we can now conclude the call.
This concludes today's conference call. You may now disconnect.